Alternative splicing in cardiomyopathy
Author:
Funder
Biotechnology and Biological Sciences Research Council
Publisher
Springer Science and Business Media LLC
Subject
Molecular Biology,Structural Biology,Biophysics
Link
http://link.springer.com/article/10.1007/s12551-018-0439-y/fulltext.html
Reference107 articles.
1. Ames EG, Lawson MJ, Mackey AJ, Holmes JW (2013) Sequencing of mRNA identifies re-expression of fetal splice variants in cardiac hypertrophy. J Mol Cell Cardiol 62:99–107. https://doi.org/10.1016/j.yjmcc.2013.05.004
2. Anderson PA, Malouf NN, Oakeley AE, Pagani ED, Allen PD (1991) Troponin T isoform expression in humans. A comparison among normal and failing adult heart, fetal heart, and adult and fetal skeletal muscle. Circ Res 69:1226–1233
3. Aufiero S et al (2018) Cardiac circRNAs arise mainly from constitutive exons rather than alternatively spliced exons. RNA. https://doi.org/10.1261/rna.064394.117
4. Barry SP, Davidson SM, Townsend PA (2008) Molecular regulation of cardiac hypertrophy. Int J Biochem Cell Biol 40:2023–2039. https://doi.org/10.1016/j.biocel.2008.02.020
5. Beqqali A et al (2016) A mutation in the glutamate-rich region of RBM20 causes dilated cardiomyopathy through missplicing of titin and impaired Frank-Starling mechanism. Cardiovasc Res. https://doi.org/10.1093/cvr/cvw192
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